Nogo receptor antagonizes p75NTR-dependent motor neuron death
نویسندگان
چکیده
منابع مشابه
Nogo receptor antagonizes p75NTR-dependent motor neuron death.
The Nogo-66 receptor (NgR) plays a critical role in restricting axon regeneration in the central nervous system. This inhibitory action is in part mediated by a neuronal receptor complex containing p75NTR, a multifunctional receptor also well known to trigger cell death upon binding to neurotrophins such as NGF. In the present study, we show that Pep4 and NEP1-40, which are two peptides derived...
متن کاملNeuron-type-specific signaling by the p75NTR death receptor is regulated by differential proteolytic cleavage.
Signaling by the p75 neurotrophin receptor (p75(NTR), also known as NGFR) is often referred to as cell-context dependent, but neuron-type-specific signaling by p75(NTR) has not been systematically investigated. Here, we report that p75(NTR) signals very differently in hippocampal neurons (HCNs) and cerebellar granule neurons (CGNs), and we present evidence indicating that this is partly control...
متن کاملLGI1 is a Nogo receptor 1 ligand that antagonizes myelin-based growth inhibition.
Mutations in leucine-rich glioma inactivated (LGI1) are a genetic cause of autosomal dominant temporal lobe epilepsy with auditory features. LGI1 is a secreted protein that shares homology with members of the SLIT family, ligands that direct axonal repulsion and growth cone collapse, and we therefore considered the possibility that LGI1 may regulate neuronal process extension or growth cone col...
متن کاملTrkA mediates developmental sympathetic neuron survival in vivo by silencing an ongoing p75NTR-mediated death signal
Developmental sympathetic neuron death is determined by functional interactions between the TrkA/NGF receptor and the p75 neurotrophin receptor (p75NTR). A key question is whether p75NTR promotes apoptosis by directly inhibiting or modulating TrkA activity, or by stimulating cell death independently of TrkA. Here we provide evidence for the latter model. Specifically, experiments presented here...
متن کاملOligodendrocytes contribute to motor neuron death in ALS via SOD1-dependent mechanism.
Oligodendrocytes have recently been implicated in the pathophysiology of amyotrophic lateral sclerosis (ALS). Here we show that, in vitro, mutant superoxide dismutase 1 (SOD1) mouse oligodendrocytes induce WT motor neuron (MN) hyperexcitability and death. Moreover, we efficiently derived human oligodendrocytes from a large number of controls and patients with sporadic and familial ALS, using tw...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Proceedings of the National Academy of Sciences
سال: 2008
ISSN: 0027-8424,1091-6490
DOI: 10.1073/pnas.0703842105